دورية أكاديمية
Emodin alleviates lung ischemia–reperfusion injury by suppressing gasdermin D‐mediated pyroptosis in rats
العنوان: | Emodin alleviates lung ischemia–reperfusion injury by suppressing gasdermin D‐mediated pyroptosis in rats |
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المؤلفون: | Tao Jin, Fen Ai, Jin Zhou, Lin Kong, Zhangming Xiong, Dingping Wang, Ruilin Lu, Zhen Chen, Muxi Zhang |
المصدر: | The Clinical Respiratory Journal, Vol 17, Iss 3, Pp 241-250 (2023) |
بيانات النشر: | Wiley, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Diseases of the respiratory system |
مصطلحات موضوعية: | emodin, gasdermin D, lung ischemia–reperfusion, NLRP3, pyroptosis, Diseases of the respiratory system, RC705-779 |
الوصف: | Abstract Background Pyroptosis refers to programmed cell death associated with inflammation. Emodin has been reported to alleviate lung injuries caused by various pathological processes and attenuate ischemia–reperfusion (I/R) injuries in diverse tissues. Methods Lewis rats were assigned into the sham, the I/R, and the I/R + emodin groups. Emodin and phosphate‐buffered saline were intraperitoneally injected into rats of the emodin group and I/R group for 30 min, respectively. These rats were then subjected to left thoracotomy followed by 90‐min clamping of the left hilum and 120‐min reperfusion. Sham‐operated rats underwent 210‐min ventilation. Lung functions, histological changes, lung edema, and cytokine levels were assessed. Protein levels were measured by western blotting. Immunofluorescence staining was conducted to evaluate pyroptosis. Results Emodin alleviated the I/R‐induced lung dysfunction, lung damages, and inflammation. Protective effects of emodin against I/R‐mediated endothelial pyroptosis was observed in vivo and in vitro. Mechanistically, emodin inactivated the TLR4/MyD88/NF‐κB/NLRP3 pathway. Conclusion Emodin attenuates lung ischemia–reperfusion injury by inhibiting GSDMD‐mediated pyroptosis in rats. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1752-699X 1752-6981 |
Relation: | https://doaj.org/toc/1752-6981; https://doaj.org/toc/1752-699X |
DOI: | 10.1111/crj.13582 |
URL الوصول: | https://doaj.org/article/28875cb3746047a5bf9bfce0e023608d |
رقم الأكسشن: | edsdoj.28875cb3746047a5bf9bfce0e023608d |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 1752699X 17526981 |
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DOI: | 10.1111/crj.13582 |